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PubMed1978

Effect of cI repressor level on thymineless and spontaneous induction; specificity of lambda RNA transcription.

To determine the role of the cI repressor in induction provoked by thymine deprivation, we have analyzed lambda messenger RNA made during and the effect of cI repressor levels on thymineless induction. During thymineless induction, the l- and r-strand transcription of lambda is restricted to the "early" and "delayed early" RNA. This transcriptional pattern is similar to that reported for lambda mutants defective in DNA synthesis. "Late" r-strand transcription requires the addition of thymine. A decrease (to less than 10% of 0 time) in the amount of exogenous label (3H-uridine) incorporated into total RNA by the time of maximum thymineless induction was observed. Since subsequent burst sizes are not diminished by the thymine deprivation and competition experiments show that the amount of lambda message RNA present is at least as great as that in heat induced lambda cI857 lysogens, this decrease must involve either enlarged uridine pool sizes or decreased entry of label. The introduction into the lambda lysogen of a plasmid (pKB252) carrying the lambda cI gene prevents (1) the thymineless induction of lambda (curing the plasmid restores thymineless induction) and, (2) the appearance of both spontaneously induced cells and free phage. Thus, thymineless induction is dependent on the level of cI repressor and spontaneous induction also appears to be the consequence of lowered repressor levels in lambda lysogens.

Coliphages↗
PubMed1998

Single vital capacity inhalational anaesthetic induction in adults--isoflurane vs sevoflurane.

PURPOSE: To evaluate whether isoflurane is as suitable as sevoflurane for the single vital capacity breath (VCB) method of inhalational induction in patients premedicated with midazolam. METHODS: A randomised, controlled, double-blind study involving 67 ASA I-II patients aged between 18-50 yr undergoing elective surgery under general anaesthesia. All participants received premedication with 0.03 mg.kg-1 midazolam i.v. Using a primed circle absorber circuit, inhalational induction of anaesthesia was performed with the single VCB method using either isoflurane 3.5% or sevoflurane 7.5% in nitrous oxide 67% in oxygen, representing approximately equivalent MAC-multiples of 3.6 MAC. Isoflurane was compared with sevoflurane in terms of rapidity, efficacy, safety and acceptability of induction. RESULTS: With the single VCB method, sevoflurane produced a faster (45 +/- 21 vs 71 +/- 22 sec, P < 0.01), more successful (100% vs 75.8%, P < 0.01) induction of anaesthesia, with fewer induction-related complications (11.8% vs 84.8%, P < 0.01) than did isoflurane. There was also greater patient acceptability of induction with sevoflurane (76.4% vs 42.4%, P < 0.05). CONCLUSION: In adults given midazolam premedication, isoflurane is not as suitable as sevoflurane for single VCB inhalational anaesthetic induction technique as it is associated with slower, more complicated induction and less patient acceptability.

Adolescent↗
PubMed1999

Risk assessment for cancer induction after low- and high-LET therapeutic irradiation.

The risk of induction of a second primary cancer after a therapeutic irradiation with conventional photon beams is well recognized and documented. However, in general, it is totally overwhelmed by the benefit of the treatment. The same is true to a large extent for the combinations of radiation and drug therapy. After fast neutron therapy, the risk of induction of a second cancer is greater than after photon therapy. Neutron RBE increases with decreasing dose and there is a wide evidence that neutron RBE is greater for cancer induction (and for other late effects relevant in radiation protection) than for cell killing. Animal data on RBE for tumor induction are reviewed, as well as other biological effects such as life shortening, malignant cell transformation in vitro, chromosome aberrations, genetic effects. These effects can be related, directly or indirectly, to cancer induction to the extent that they express a "genomic" lesion. Almost no reliable human epidemiological data are available so far. For fission neutrons a RBE for cancer induction of about 20 relative to photons seems to be a reasonable assumption. For fast neutrons, due to the difference in energy spectrum, a RBE of 10 can be assumed. After proton beam therapy (low-LET radiation), the risk of secondary cancer induction, relative to photons, can be divided by a factor of 3, due to the reduction of integral dose (as an average). The RBE of heavy-ions for cancer induction can be assumed to be similar to fission neutrons, i.e. about 20 relative to photons. However, after heavy-ion beam therapy, the risk should be divided by 3, as after proton therapy due to the excellent physical selectivity of the irradiation. Therefore a risk 5 to 10 times higher than photons could be assumed. This range is probably a pessimistic estimate for carbon ions since most of the normal tissues, at the level of the initial plateau, are irradiated with low-LET radiation.

Alpha Particles↗
PubMed2004

Effects of oral atenolol on volatile anesthetic induction with sevoflurane in adults.

PURPOSE: To determine whether premedication with a beta-blocker can bring about a more rapid and smooth induction of anesthesia, we investigated the effect of oral premedication with atenolol on volatile anesthetic induction with sevoflurane by monitoring the cardiac output (CO) and bispectral (BIS) index. METHODS: Twenty-four patients undergoing general anesthesia with endotracheal intubation were randomly divided into two groups: a control group ( n = 12) and a beta-blocker group ( n = 12). Each patient in the beta-blocker group was premedicated with oral atenolol 25 mg 1 h before the induction of anesthesia. Anesthesia was induced by the repeated vital capacity technique with 5% sevoflurane and 66% nitrous oxide. The trachea was intubated 5 min after sevoflurane exposure. The CO and BIS index, as well as the induction time and specific side effects of induction (e.g., movement of limbs), were recorded. RESULTS: There were no significant differences in induction time and specific side effects between the groups. The downward-sloping part of the BIS index curve in the beta-blocker group (mean, 2.9 +/- 0.2) was significantly sharper than that in the control group (2.5 +/- 0.2), and the BIS index after induction of anesthesia was significantly lower in the beta-blocker group (21.0 +/- 2.2) than in the control group (24.2 +/- 2.0). CO in the beta-blocker group was significantly lower than in the control group during the study period. The hemodynamic changes caused by endotracheal intubation were inhibited in the beta-blocker group but not in the control group. CONCLUSION: Oral premedication with 25 mg of atenolol provides a more rapid decrease in BIS index and is recommended for use in stable volatile anesthetic induction with sevoflurane.

Administration, Oral↗
PubMed1988

Glycoprotein biosynthesis in B lymphocytes: induction of protein N-glycosylation, RNA synthesis, and DNA synthesis by phorbol ester plus ionomycin is blocked by protein kinase inhibitors.

The combination of phorbol 12-myristate 13-acetate (PMA) and ionomycin produces a dramatic increase in the incorporation of [2-3H]mannose into Glc3Man9GlcNAc2-P-P-dolichol and glycoprotein, and the induction of RNA and DNA synthesis in murine splenic B lymphocytes (B cells). The kinetics of the induction processes and the concentrations of PMA and ionomycin required for the optimal response have been defined. While the levels of induction of RNA and DNA synthesis by PMA + ionomycin were similar to the mitogenic response to bacterial lipopolysaccharide, activation by PMA and the calcium ionophore resulted in a threefold higher stimulation in dolichol-linked oligosaccharide biosynthesis and protein N-glycosylation. These results indicate that all signalling mechanisms that trigger RNA and DNA synthesis may not be sufficient to produce maximal induction of the N-glycosylation apparatus. 1-(5-Isoquinolinesulfonyl)-2-methylpiperazine (H-7), a potent protein kinase C inhibitor, prevented the induction of protein N-glycosylation activity (IC50 = 11 microM), as well as RNA (IC50 = 18 microM) and DNA synthesis (IC50 = 12 microM), two common indices of B cell activation. N-[2-(Methylamino)ethyl]-5-isoquinolinesulfonamide (H-8) also inhibited the induction of oligosaccharide-lipid intermediate, glycoprotein, RNA, and DNA synthesis, but required higher concentrations than H-7 for 50% inhibition. N-(2-Guanidinoethyl)-5-isoquinolinesulfonamide (HA1004), a potent inhibitor of cyclic nucleotide-dependent protein kinases, had little effect on the activation of the B cell metabolic processes. The H-7-sensitive reactions involved in the induction of RNA and DNA synthesis occurred within 4 h, but induction of lipid intermediate and glycoprotein biosynthesis remained sensitive to H-7 for 10 h after exposure to PMA and ionomycin. Direct in vitro assays in the presence of 0.6% Brij 58 reveal that a cytosolic, phospholipid-dependent protein kinase activity is translocated to a membrane site(s) after treatment with PMA and ionomycin, and the translocated protein kinase is sensitive to H-7. The relative order of potency of the protein kinase inhibitors on the metabolic processes strongly supports the hypothesis that protein kinase C, acting synergistically with Ca2+ mobilization, plays a key regulatory role in the early stages of B cell activation. The synthesis of oligosaccharide-lipid intermediates and protein N-glycosylation are also shown to be induced in B cells activated by PMA + ionomycin.

Animals↗
PubMed1992

Different thresholds of HSP70 and HSC70 heat shock mRNA induction in post-ischemic gerbil brain.

Thresholds of induction of heat shock protein (HSP) 70 and heat shock cognate protein (HSC) 70 mRNAs after transient global ischemia in gerbil brain were investigated by in situ hybridization using cloned cDNA probes selective for each mRNA species. In sham control brain, HSP70 mRNA was little present, while HSC70 mRNA was present in most cell populations. A 0.5-min occlusion of bilateral common carotid arteries did not affect the amount of HSP70 and HSC70 mRNAs. The selective induction of HSC70 mRNA was observed in dentate granule cells at 1 h, and in most cells of hippocampus especially dentate gyrus at 3 h after 1 min of ischemia when induction of HSP70 mRNA was not evident in the identical brain. The selective induction diminished by 2 days. However, after 2 min of ischemia, HSP70 and HSC70 mRNAs were induced together in hippocampal cells from 1 h of the reperfusion, and the co-induction prolonged in CA1 cells until 2 days. Body temperatures monitored at rectum increased after the reperfusion with a peak at 30 min. The degree of increase of the body temperature was significantly higher in the case after 2-min ischemia than in the cases after 0.5- and 1-min ischemia. Although HSP70 and HSC70 mRNAs are generally co-induced in stressful conditions, our results suggest the different thresholds of the induction between HSP70 and HSC70 mRNAs after transient brain ischemia. The selective induction of HSC70 mRNA which is not accompanied by the induction of HSP70 mRNA may relate to the differences of the duration of ischemia and the degree of the increase of body temperature after ischemia.

Animals↗
PubMed1992

Induction of c-jun independent of PKC, pertussis toxin-sensitive G protein, and polyamines in quiescent SV40-transformed 3T3 T cells.

CSV3 clones of simian virus 40 large T antigen-transformed murine 3T3 T cells can be made quiescent as part of a differentiation process. In these quiescent cells, insulin- and vanadate-induced mitogenesis are both associated with the induction of the c-jun proto-oncogene (Wang and Scott 1991 J. Cell. Physiol. 147, 102-110; Wang et al. 1991 Cell Growth Differ. 2, 645-652). The current studies were therefore designed to compare the early signal transduction pathways employed by insulin and vanadate to regulate c-jun expression. In quiescent CSV3-1 cells, down-regulation of protein kinase C by prolonged exposure to 12-O-tetra-decanoylphorbol-13-acetate or inhibition of protein kinase C activity by treatment with the protein kinase C antagonist staurosporine is shown not to affect c-jun induction by insulin or vanadate. This suggests that both insulin and vanadate act in a protein kinase C-independent manner. Insulin's effect on c-jun induction does, however, involve a G protein because insulin's effect can be inhibited by pertussis toxin. In contrast, vanadate induction of c-jun is not affected by pertussis toxin. Genistein, a general tyrosine kinase inhibitor, can inhibit the ability of vanadate to induce c-jun but it does not inhibit insulin's effect. Finally, the depletion of polyamines, particularly spermidine, by DL-alpha-difluoromethylornithine treatment also prevents c-jun induction by insulin but DL-alpha-difluoromethylornithine treatment has no effect on c-jun induction by vanadate. These observations indicate that the c-jun induction by insulin and vanadate in CSV3-1 cells is mediated by different signal transduction mechanisms. Together with our previously published data, these results suggest that c-jun can be induced independent of protein kinase C activation, without involvement of pertussis toxin-sensitive G protein, independent of induction of c-fos, and without expression of high levels of intracellular polyamines.

3T3 Cells↗
PubMed1979

Ultraviolet radiation induction of endogenous murine type C virus.

Induction of endogenous type C RNA virus occurred following exposure of mouse cells to ultraviolet radiation. Irradiation of A1-2 cells, derived from the BALB/c mouse, induced endogenous xenotropic type C virus as determined by infectious center focus-forming assay on normal rat-kidney (NRK) cells. Viral induction by UV radiation was compared to that for the halogenated pyrimidines, 5-iodo-2-deoxyuridine (IdU) and 5-bromo-2-deoxyuridine (BrdU). Although the fraction of A1-2 cells induced to release virus by UV radiation (0.17%) was less than that observed for IdU (3.0%) and BrdU (0.46%), use of the sensitive infectious center assay demonstrated reproducible UV induction. Dose-response studies showed that the level of viral induction by UV was dependent upon cellular UV exposure. Study of A1-2 cell survival following irradiation showed that optimum viral induction occurred at a UV exposure corresponding to the edge of the shoulder of the survival curve, suggesting that UV sensitivity of the host cell may be a factor limiting the level of induction. Since less radiation was required for viral induction than for inactivation of colony-forming ability, viral induction may be a more sensitive dosimeter of in vitro UV bioeffects than cell survival for this system.

Bromodeoxyuridine↗
PubMed1987

Chromosomal instability in mutagen-sensitive mutants isolated from mouse lymphoma L5178Y cells. II. Abnormal induction of sister-chromatid exchanges and chromosomal aberrations by mutagens in an ionizing radiation-sensitive mutant (M10) and an alkylating agent-sensitive mutant (MS1).

To determine the mutual relationships between cell survival and induction of sister-chromatid exchanges (SCEs) as well as chromosomal aberrations (CAs), mutagen-induced SCEs and CAs were analyzed in an ionizing radiation-sensitive mutant (M10) and an alkylating agent-sensitive mutant (MS 1) isolated from mouse lymphoma L5178Y cells. The levels of CA induction in both mutants strictly corresponded to the sensitivity to lethal effects of mutagens, except that caffeine-induced CAs in M10 are considerably lower than those in L5178Y. The results clearly indicate that except for caffeine-induced CAs in M10, mutagen-induced lethal lesions are responsible for CA induction. In contrast, SCE induction in mutants was complicated. In M10, hypersensitive to killing by gamma-rays, methyl methanesulfonate (MMS), and 4-nitroquinoline 1-oxide (4NQO), but not sensitive to UV or caffeine, the frequency of SCEs induced by gamma-rays was barely higher than that in L5178Y, and the frequencies of MMS- and UV-induced SCEs were similar to those in L5178Y, but 4NQO- and caffeine-induced SCEs were markedly lower than those in L5178Y. MS 1, which is hypersensitive to MMS and caffeine, but not sensitive to UV or 4NQO, responded to caffeine with an enhanced frequency of SCEs and had a normal frequency of MMS-induced SCEs, but a reduced frequency of UV- and 4NQO-induced SCEs. Thus, susceptibility to SCE induction by mutagens is not necessarily correlated with sensitivity of mutants to cell killing and/or CA induction by mutagens. Furthermore, the spontaneous levels of SCEs are lower in M10 and higher in MS 1 than that in L5178Y (Tsuji et al., 1987). Based on these results, we speculate that M10 may be partially defective in the processes for the formation of SCEs caused by mutagens. On the other hand, MS 1 may modify SCE formation-related lesions induced by UV and 4NQO to some repair intermediates that do not cause SCE formation. In addition, MMS-induced lethal lesions in MS 1 may not be responsible for SCE induction whereas caffeine-induced lethal lesions are closely correlated with SCE induction. Thus, the lesions or mechanisms involved in SCE production are in part different from those responsible for cell lethality or CA production.

4-Nitroquinoline-1-oxide↗
PubMed1990

Disappearance of grating induction at scotopic luminances.

The dependence of grating induction magnitude on retinal illuminance was examined in two subjects. Grating induction magnitude, as determined using the cancellation technique of McCourt, declines monotonically with decreasing retinal illuminance, effectively disappearing at a value of 0.3-0.5 phot td. In a second experiment, sensitivity differences for test lights of 500 and 600 nm were measured as a function of background illuminance in order to gauge the luminance operating range for grating induction with respect to duplex photoreceptor function. Cancelling contrast (and hence grating induction magnitude) fell below detection threshold contrast at retinal illuminances coinciding with the transition from photopic to scotopic visual function. In a third experiment, spatial contrast sensitivity was measured using both spatially extended (10 degrees) and truncated (2 degrees) sinewave gratings at frequencies below 2 c/deg, at three values of retinal illuminance. Illuminance values corresponded to those where grating induction magnitude was, as determined from the first experiment, either maximal, intermediate or negligible. Similar to grating induction, the strength of lateral inhibition, as indexed by the slope of the low-frequency decline in contrast sensitivity, is progressively reduced with decreasing retinal illuminance, particularly for the 2 degree field. There was, however, using the same criteria, evidence of lateral inhibition at a value of retinal illuminance which did not support grating induction. The implications of these results are discussed with respect to classical brightness contrast phenomena, recent neuroanatomical and neurophysiological evidence of segregated parvo- and magnocellular mediated contrast processing systems, and with results from previous studies of the grating induction effect.

Contrast Sensitivity↗
PubMed1991

Sputum induction for the diagnosis of pulmonary disease in HIV positive patients.

We prospectively compared sputum induction with bronchoalveolar lavage (BAL) in HIV positive patients presenting with acute respiratory episodes and also assessed the effects of using an experienced respiratory physiotherapist on the diagnostic yield from induced sputum. One hundred and fifty-one consecutive patients underwent sputum induction, in 96 the procedure was supervised by nursing and medical staff with no specific expertise (group I); in 55 patients a physiotherapist supervised sputum induction (group 2). Nine patients refused BAL having undergone sputum induction. Of the remaining 142 patients sputum induction failed (no sample expectorated) in 28 patients (25 from group 1 and three from group 2), the sample was inadequate (the material expectorated was not from the lower respiratory tract) in 29, and was adequate in 85 patients. Pneumocystis carinii was diagnosed in 82 patients (51 from group 1 and 31 from group 2). The sensitivity of induced sputum for the diagnosis of P. carinii was 13% and of BAL was 77%. In the subgroup of patients with an adequate induced sputum sample, the sensitivity of induced sputum was 28% and of BAL was 73%. Of the remaining 60 patients, 27 had other diagnoses made by induced sputum and BAL (eight patients), BAL only (15 patients) and induced sputum only (four patients). Eleven patients had bronchitis and responded to oral antibiotics. In 22 patients induced sputum and BAL were negative; alternative diagnoses were established by lung biopsy or by culture of blood, urine or CSF. During sputum induction, 15 patients had nausea and vomiting, eight became dyspnoeic, three had intractable cough and one developed acute bronchoconstriction; 17 patients found the procedure unpleasant. Compared with BAL, induced sputum has a lower diagnostic yield for P. carinii and other pathogens. Use of experienced, dedicated personnel increases the number of successful attempts at sputum induction but does not increase the diagnostic yield. Fibreoptic bronchoscopy and bronchoalveolar lavage remain necessary for patients with negative results from induced sputum and those whose disease course is at variance with the diagnosis made by sputum induction.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Involvement of calmodulin- and protein kinase C-related mechanism in an induction process of peroxisomal fatty acid oxidation-related enzymes by hypolipidemic peroxisome proliferators.

Trifluoperazine, a calmodulin antagonist, suppressed the clofibric acid-evoked induction of the peroxisomal cyanide-insensitive fatty acyl-CoA oxidizing system and carnitine acetyltransferase in rat liver and also in cultured rat hepatocytes. H-7, a potent inhibitor of protein kinase C, also suppressed the induction of these enzymes by clofibric acid, bezafibrate, Wyl4,643 or mono(2-ethylhexyl)phthalate in cultured rat hepatocytes. This suppressive effect was also confirmed by the protein composition of hepatocytes treated with clofibric acid and these antagonists, where the increase in the amount of peroxisomal bifunctional enzyme by peroxisome proliferator was markedly suppressed by above two antagonists. Profile of the time-dependent changes in the activities of the two enzymes after clofibric acid treatment showed that there might be two phases in the induction process. The initial phase (0-3 days after the treatment) showed a relative low inducing rate and subsequent phase (3-5 days after the treatment) showed an abrupt induction. The suppressive effect of the above two antagonists was significant in the later phase. In a time course study of the induction process of peroxisomal catalase, bifunctional enzyme or 69 kDa integral membrane protein using immunochemical detection, the induction of the membrane protein by clofibric acid was delayed compared with that of the bifunctional enzyme, where the induction was inhibited almost completely by nicardipine. These experimental results suggest that calmodulin- and protein kinase C-dependent processes play an important role in the process of marked induction of peroxisomal enzymes and membrane protein by drugs in rat liver.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1989

Comparison of immediate versus day to day variability of ventricular tachycardia induction by programmed stimulation.

The use of programmed stimulation to assess long-term oral antiarrhythmic drug efficacy for ventricular tachycardia is complicated by the fact that mode of ventricular tachycardia induction varies from day to day in the absence of drug therapy. The purpose of this prospective study was to assess whether mode of ventricular tachycardia induction is more reproducible within one study than from day to day. Thirty-nine consecutive patients with documented sustained ventricular tachyarrhythmias secondary to coronary artery disease underwent three inductions of ventricular tachycardia at 15 min intervals in the absence of drug therapy. A stimulation protocol in which the only major variable was the number of extrastimuli required for tachycardia induction was used. Subsequent day to day variability in mode of tachycardia induction was also assessed in the same patients at two further drug-free inductions at intervals of 5 +/- 2 days. The number of extrastimuli required for tachycardia induction was significantly more reproducible at the immediate repeat studies than from day to day (69% of patients versus 31%, p less than 0.01). From these data, probability tables were derived that show the likelihood that changes in inducibility at subsequent tachycardia inductions are due to chance. The QRS configuration of induced ventricular tachycardia was also more reproducible at the immediate studies (64% versus 26%, p less than 0.01). Basic electrophysiologic and stimulation variables differed over a significantly wider range from day to day than at the immediate studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Catecholamine responses to anesthetic induction with fentanyl and sufentanil.

In a randomized study, the authors examined the changes in plasma epinephrine and norepinephrine concentrations associated with induction of anesthesia and surgery in 33 patients with good ventricular function undergoing elective coronary artery surgery. After premedication with morphine and scopolamine, patients received either fentanyl, 100 micrograms/kg (n = 16), or sufentanil, 15 micrograms/kg, (n = 17), intravenously (IV), over 10 minutes to induce anesthesia. Metocurine, 0.42 mg/kg, IV, produced muscle relaxation. Arterial blood for plasma catecholamine determinations was drawn prior to induction, every two minutes throughout induction, one minute following endotracheal intubation, and one minute after sternotomy. Plasma epinephrine concentration was unchanged with either induction agent. Plasma norepinephrine concentration increased significantly after administration of either narcotic, peaked between six and ten minutes into induction, and returned to the preinduction value after intubation. Induction-related changes in arterial pressure and pulmonary capillary wedge pressure were significantly correlated with changes in the logarithm of plasma norepinephrine concentration. Similar degrees of endogenous norepinephrine release appear to accompany induction with equipotent doses of fentanyl and sufentanil in patients premedicated with morphine and scopolamine. Norepinephrine release may influence the hemodynamic response to induction with narcotics.

Anesthesia, Intravenous↗
PubMed1994

Induction of the genes RAD54 and RNR2 by various DNA damaging agents in Saccharomyces cerevisiae.

The relationship between the induction of the genes RAD54 and RNR2 and the induction and repair of specific DNA lesions was studied in the yeast Saccharomyces cerevisiae using Rad54-lacZ and RNR2-lacZ fusion strains. Gene induction was followed by measuring beta-galactosidase activity. At comparable levels of furocoumarin-DNA photoadducts, RAD54 was more effectively induced by bifunctional than by monofunctional furocoumarins indicating that mixtures of monoadducts (MA) and interstrand cross-links (CL) provide a stronger inducing signal than MA. RNR2 induction kinetics were measured in relation to cell growth and survival responses after treatment with the furocoumarins 8-methoxypsoralen (8-MOP), 5-methoxypsoralen (5-MOP), 3-carbethoxypsoralen (3-CPs), 7-methyl-pyrido[3,4-c]psoralen (MePyPs) and 4,4',6-trimethylangelicin (TMA), benzo[a]pyrene (B(a)P and 1,6-dioxapyrene (1,6-DP) plus UVA, 254 nm UV radiation and cobalt-60 gamma-radiation. Induction of RNR2 took place during the DNA repair period before resumption of cell growth and clearly increased with increasing equitoxic dose levels. Treatments with furocoumarin plus 365 nm radiation (UVA) and 254 nm (UV) radiation were effective inducers whereas gene induction was relatively weak after gamma-radiation and absent after the induction of oxidative damage by B(a)P and 1,6-DP and UVA. The results suggest that it is the specific processing of different DNA lesions that determines the potency of the induction signal. Apparently, DNA lesions such as CL, and probably also closely located MA or pyrimidine dimers in opposite DNA strands involving the formation of double-strand breaks as repair intermediates, are most effective inducers.

DNA Helicases↗
PubMed2004

Growth factor combination for chondrogenic induction from human mesenchymal stem cell.

During the last decade, many strategies for cartilage engineering have been emerging. Stem cell induction is one of the possible approaches for cartilage engineering. The mesenchymal stem cells (MSCs) with their pluripotency and availability have been demonstrated to be an attractive cell source. It needs the stimulation with cell growth factors to make the multipluripotent MSCs differentiate into chondrogenic lineage. We have shown particular patterns of in vitro chondrogenesis induction on human bone marrow MSCs (hBMSCs) by cycling the growth factors. The pellet cultures of hBMSCs were prepared for chondrogenic induction. Growth factors: TGF-beta3, BMP-6, and IGF-1 were used in combination for cell induction. Gene expression, histology, immunohistology, and real-time PCR methods were measured on days 21 after cell induction. As shown by histology and immunohistology, the induced cells have shown the feature of chondrocytes in their morphology and extracellular matrix in both inducing patterns of combination and cycling induction. Moreover, the real-time PCR assay has shown the expression of gene markers of chondrogenesis, collagen type II and aggrecan. This study has demonstrated that cartilage tissue can be created from bone marrow mesenchymal stem cells. Interestingly, the combined growth factors TGF-beta3 and BMP-6 or TGF-beta3 and IGF-1 were more effective for chondrogenesis induction as shown by the real-time PCR assay. The combination of these growth factors may be the important key for in vitro chondrogenesis induction.

Cartilage↗
PubMed2005

A comparison of oral and vaginal misoprostol for induction of labor.

OBJECTIVE: The aim of the study is to compare the efficacy and safety of oral (100 microg) and vaginal (50 microg) misoprostol for labor induction. STUDY DESIGN: Ninety-nine patients with indications for labor induction randomly received 100 microg oral misoprostol every 4 h or 50 microg vaginal misoprostol every 4 h, using maximum six doses. Mean induction to delivery interval, mode of delivery, rates of tachysystole, hypertonus and hyperstimulation syndrome, oxytocin use, number of doses used, failed induction rate and neonatal outcomes were compared for the two groups. RESULTS: Mean dose of misoprostol used for oral and vaginal misoprostol groups were 2.17+/-1.35 and 1.91+/-0.94, respectively (p=0.65). There were two failed inductions in the oral (4%) and one failed induction (2.5%) in the vaginal group after a total of six doses of misoprostol (p=0.58). There was no significant difference for the mean induction to delivery interval, to the beginning of active phase interval, active phase duration, second stage duration and the number of women who received oxytocin for induction or augmentation between the two groups (p>0.05). There were also no significant differences for intrapartum complications and neonatal outcomes between the oral and vaginal misoprostol groups (p>0.05). CONCLUSION: Our findings indicate that, in a closely supervised hospital setting with adequate monitoring, 100 microg oral misoprostol has the potential to induce labor as safely and effectively as its 50 microg vaginal analogue. As oral use of the drug is easier for both the patient and the doctor, oral misoprostol will probably be more preferable than the vaginal route.

Abortifacient Agents, Nonsteroidal↗
PubMed2005

Protein production by auto-induction in high density shaking cultures.

Inducible expression systems in which T7 RNA polymerase transcribes coding sequences cloned under control of a T7lac promoter efficiently produce a wide variety of proteins in Escherichia coli. Investigation of factors that affect stability, growth, and induction of T7 expression strains in shaking vessels led to the recognition that sporadic, unintended induction of expression in complex media, previously reported by others, is almost certainly caused by small amounts of lactose. Glucose prevents induction by lactose by well-studied mechanisms. Amino acids also inhibit induction by lactose during log-phase growth, and high rates of aeration inhibit induction at low lactose concentrations. These observations, and metabolic balancing of pH, allowed development of reliable non-inducing and auto-inducing media in which batch cultures grow to high densities. Expression strains grown to saturation in non-inducing media retain plasmid and remain fully viable for weeks in the refrigerator, making it easy to prepare many freezer stocks in parallel and use working stocks for an extended period. Auto-induction allows efficient screening of many clones in parallel for expression and solubility, as cultures have only to be inoculated and grown to saturation, and yields of target protein are typically several-fold higher than obtained by conventional IPTG induction. Auto-inducing media have been developed for labeling proteins with selenomethionine, 15N or 13C, and for production of target proteins by arabinose induction of T7 RNA polymerase from the pBAD promoter in BL21-AI. Selenomethionine labeling was equally efficient in the commonly used methionine auxotroph B834(DE3) (found to be metE) or the prototroph BL21(DE3).

Amino Acids↗